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A novel yeast gene, THO2 , is involved in RNA pol II transcription and provides new evidence for transcriptional elongation‐associated recombination
Author(s) -
Piruat José I.,
Aguilera Andrés
Publication year - 1998
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/17.16.4859
Subject(s) - biology , transcription (linguistics) , recombination , elongation , rna polymerase ii , genetics , gene , rna , saccharomyces cerevisiae , yeast , gene expression , promoter , materials science , ultimate tensile strength , metallurgy , philosophy , linguistics
We have identified two novel yeast genes, THO1 and THO2 , that partially suppress the transcription defects of hpr1 Δ mutants by overexpression. We show by in vivo transcriptional and recombinational analysis of tho2 Δ cells that THO2 plays a role in RNA polymerase II (RNA pol II)‐dependent transcription and is required for the stability of DNA repeats, as previously shown for HPR1 . The tho2 Δ mutation reduces the transcriptional efficiency of yeast DNA sequences down to 25% of the wild‐type levels and abolishes transcription of the lacZ sequence. In addition, tho2 Δ causes a strong increase in the frequency of recombination between direct repeats (>2000‐fold above wild‐type levels). Some DNA repeats cannot even be maintained in the cell. This hyper‐recombination phenotype is dependent on transcription and is not observed in DNA repeats that are not transcribed. The higher the impairment of transcription caused by tho2 Δ, the higher the frequency of recombination of a particular DNA region. The tho2 Δ mutation also increases the frequency of plasmid loss. Our work not only identifies a novel yeast gene, THO2 , with similar function to HPR1 , but also provides new evidence for transcriptional blocks as a source of recombination. We propose that there is a set of proteins including Hpr1p and Tho2p, in the absence of which RNA pol II transcription is stalled or blocked, causing genetic instability.